Ecg
Upcoming SlideShare
Loading in...5
×

Like this? Share it with your network

Share

Ecg

  • 2,320 views
Uploaded on

 

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
No Downloads

Views

Total Views
2,320
On Slideshare
2,320
From Embeds
0
Number of Embeds
0

Actions

Shares
Downloads
258
Comments
0
Likes
3

Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide
  • Acute Myocardial Infarction after Blunt Chest Trauma in A Young Man (2002. 8) Àü³²´ë ¼øȯ±â ³»°ú Á¤¸íÈ£ ±³¼ö   Case Coronary artery injury rarely occurs after blunt chest trauma, but it can lead to extensive myocardial infarction and be frequently overlooked, and may cause severe ventricular dysfunction. A 16-year-old man presented with comatose mental state and dyspnea. He ran into guardrail while riding a motorcycle. When he arrived at the hospital, he was in comatose mental state and had a rapid respiration rate. In routine examination, his electrocardiogram showed Q wave and 2mm ST segment elevation in V1-6. The cardiac enzymes were also elevated: CK-MB was 300, and cTnI 5.7ng/ml. Due to his comatose mental state he could not complain of any chest pain. Two-dimensional echocardiography showed anteroseptal akinesia in the left ventricle with severely depressed LV function (EF=28%). He could not receive any anticoagulation or thrombolytic therapy because of his brain lesion. Three weeks later, his mental state improved and we could try an invasive study. A diagnostic coronary angiogram revealed total occlusion in the proximal LAD with collaterals from RCA and LCX. Under bilateral angiogram we could successfully pass the guide wire through the lesion, but only a 1.5mm Hayate-Pro( balloon could pass through the lesion. We dilated the balloon twice and exchanged it with a 3.0 mm balloon. Despite inflating twice, residual stenosis still remained. We deployed a 3.0(20 mm Tsunami stent in the lesion. The final angiogram showed a good coronary flow without residual stenosis. Fig.4B. Under the guidance of contralateral right coronary angiogram, guide wire was passed the lesion successfully.     Legend   Fig.1. An electrocardiogram demonstrated sinus tachycardia, Q wave and ST segment elevation over the entire precordial leads, and lead I and aVL.
  • Acute Myocardial Infarction after Blunt Chest Trauma in A Young Man (2002. 8) Àü³²´ë ¼øȯ±â ³»°ú Á¤¸íÈ£ ±³¼ö   Case Coronary artery injury rarely occurs after blunt chest trauma, but it can lead to extensive myocardial infarction and be frequently overlooked, and may cause severe ventricular dysfunction. A 16-year-old man presented with comatose mental state and dyspnea. He ran into guardrail while riding a motorcycle. When he arrived at the hospital, he was in comatose mental state and had a rapid respiration rate. In routine examination, his electrocardiogram showed Q wave and 2mm ST segment elevation in V1-6. The cardiac enzymes were also elevated: CK-MB was 300, and cTnI 5.7ng/ml. Due to his comatose mental state he could not complain of any chest pain. Two-dimensional echocardiography showed anteroseptal akinesia in the left ventricle with severely depressed LV function (EF=28%). He could not receive any anticoagulation or thrombolytic therapy because of his brain lesion. Three weeks later, his mental state improved and we could try an invasive study. A diagnostic coronary angiogram revealed total occlusion in the proximal LAD with collaterals from RCA and LCX. Under bilateral angiogram we could successfully pass the guide wire through the lesion, but only a 1.5mm Hayate-Pro( balloon could pass through the lesion. We dilated the balloon twice and exchanged it with a 3.0 mm balloon. Despite inflating twice, residual stenosis still remained. We deployed a 3.0(20 mm Tsunami stent in the lesion. The final angiogram showed a good coronary flow without residual stenosis. Fig.4B. Under the guidance of contralateral right coronary angiogram, guide wire was passed the lesion successfully.     Legend   Fig.1. An electrocardiogram demonstrated sinus tachycardia, Q wave and ST segment elevation over the entire precordial leads, and lead I and aVL.
  • Acute Myocardial Infarction after Blunt Chest Trauma in A Young Man (2002. 8) Àü³²´ë ¼øȯ±â ³»°ú Á¤¸íÈ£ ±³¼ö   Case Coronary artery injury rarely occurs after blunt chest trauma, but it can lead to extensive myocardial infarction and be frequently overlooked, and may cause severe ventricular dysfunction. A 16-year-old man presented with comatose mental state and dyspnea. He ran into guardrail while riding a motorcycle. When he arrived at the hospital, he was in comatose mental state and had a rapid respiration rate. In routine examination, his electrocardiogram showed Q wave and 2mm ST segment elevation in V1-6. The cardiac enzymes were also elevated: CK-MB was 300, and cTnI 5.7ng/ml. Due to his comatose mental state he could not complain of any chest pain. Two-dimensional echocardiography showed anteroseptal akinesia in the left ventricle with severely depressed LV function (EF=28%). He could not receive any anticoagulation or thrombolytic therapy because of his brain lesion. Three weeks later, his mental state improved and we could try an invasive study. A diagnostic coronary angiogram revealed total occlusion in the proximal LAD with collaterals from RCA and LCX. Under bilateral angiogram we could successfully pass the guide wire through the lesion, but only a 1.5mm Hayate-Pro( balloon could pass through the lesion. We dilated the balloon twice and exchanged it with a 3.0 mm balloon. Despite inflating twice, residual stenosis still remained. We deployed a 3.0(20 mm Tsunami stent in the lesion. The final angiogram showed a good coronary flow without residual stenosis. Fig.4B. Under the guidance of contralateral right coronary angiogram, guide wire was passed the lesion successfully.     Legend   Fig.1. An electrocardiogram demonstrated sinus tachycardia, Q wave and ST segment elevation over the entire precordial leads, and lead I and aVL.
  • Acute Myocardial Infarction after Blunt Chest Trauma in A Young Man (2002. 8) Àü³²´ë ¼øȯ±â ³»°ú Á¤¸íÈ£ ±³¼ö   Case Coronary artery injury rarely occurs after blunt chest trauma, but it can lead to extensive myocardial infarction and be frequently overlooked, and may cause severe ventricular dysfunction. A 16-year-old man presented with comatose mental state and dyspnea. He ran into guardrail while riding a motorcycle. When he arrived at the hospital, he was in comatose mental state and had a rapid respiration rate. In routine examination, his electrocardiogram showed Q wave and 2mm ST segment elevation in V1-6. The cardiac enzymes were also elevated: CK-MB was 300, and cTnI 5.7ng/ml. Due to his comatose mental state he could not complain of any chest pain. Two-dimensional echocardiography showed anteroseptal akinesia in the left ventricle with severely depressed LV function (EF=28%). He could not receive any anticoagulation or thrombolytic therapy because of his brain lesion. Three weeks later, his mental state improved and we could try an invasive study. A diagnostic coronary angiogram revealed total occlusion in the proximal LAD with collaterals from RCA and LCX. Under bilateral angiogram we could successfully pass the guide wire through the lesion, but only a 1.5mm Hayate-Pro( balloon could pass through the lesion. We dilated the balloon twice and exchanged it with a 3.0 mm balloon. Despite inflating twice, residual stenosis still remained. We deployed a 3.0(20 mm Tsunami stent in the lesion. The final angiogram showed a good coronary flow without residual stenosis. Fig.4B. Under the guidance of contralateral right coronary angiogram, guide wire was passed the lesion successfully.     Legend   Fig.1. An electrocardiogram demonstrated sinus tachycardia, Q wave and ST segment elevation over the entire precordial leads, and lead I and aVL.
  • Acute Myocardial Infarction after Blunt Chest Trauma in A Young Man (2002. 8) Àü³²´ë ¼øȯ±â ³»°ú Á¤¸íÈ£ ±³¼ö   Case Coronary artery injury rarely occurs after blunt chest trauma, but it can lead to extensive myocardial infarction and be frequently overlooked, and may cause severe ventricular dysfunction. A 16-year-old man presented with comatose mental state and dyspnea. He ran into guardrail while riding a motorcycle. When he arrived at the hospital, he was in comatose mental state and had a rapid respiration rate. In routine examination, his electrocardiogram showed Q wave and 2mm ST segment elevation in V1-6. The cardiac enzymes were also elevated: CK-MB was 300, and cTnI 5.7ng/ml. Due to his comatose mental state he could not complain of any chest pain. Two-dimensional echocardiography showed anteroseptal akinesia in the left ventricle with severely depressed LV function (EF=28%). He could not receive any anticoagulation or thrombolytic therapy because of his brain lesion. Three weeks later, his mental state improved and we could try an invasive study. A diagnostic coronary angiogram revealed total occlusion in the proximal LAD with collaterals from RCA and LCX. Under bilateral angiogram we could successfully pass the guide wire through the lesion, but only a 1.5mm Hayate-Pro( balloon could pass through the lesion. We dilated the balloon twice and exchanged it with a 3.0 mm balloon. Despite inflating twice, residual stenosis still remained. We deployed a 3.0(20 mm Tsunami stent in the lesion. The final angiogram showed a good coronary flow without residual stenosis. Fig.4B. Under the guidance of contralateral right coronary angiogram, guide wire was passed the lesion successfully.     Legend   Fig.1. An electrocardiogram demonstrated sinus tachycardia, Q wave and ST segment elevation over the entire precordial leads, and lead I and aVL.
  • Acute Myocardial Infarction after Blunt Chest Trauma in A Young Man ECG: Q wave and 2mm ST segment elevation in V1-6, I and avL Cardiac enzymes: CK-MB was 300, and cTnI 5.7ng/ml ECHO: anteroseptal akinesia in the LVe with severely depressed LV function (EF=28%) Angio: total occlusion in the proximal LAD with collaterals from RCA and LCX
  • Acute Myocardial Infarction after Blunt Chest Trauma in A Young Man ECG: Q wave and 2mm ST segment elevation in V1-6, I and avL Cardiac enzymes: CK-MB was 300, and cTnI 5.7ng/ml ECHO: anteroseptal akinesia in the LVe with severely depressed LV function (EF=28%) Angio: total occlusion in the proximal LAD with collaterals from RCA and LCX
  • Acute Myocardial Infarction after Blunt Chest Trauma in A Young Man ECG: Q wave and 2mm ST segment elevation in V1-6, I and avL Cardiac enzymes: CK-MB was 300, and cTnI 5.7ng/ml ECHO: anteroseptal akinesia in the LVe with severely depressed LV function (EF=28%) Angio: total occlusion in the proximal LAD with collaterals from RCA and LCX
  • Acute Myocardial Infarction after Blunt Chest Trauma in A Young Man ECG: Q wave and 2mm ST segment elevation in V1-6, I and avL Cardiac enzymes: CK-MB was 300, and cTnI 5.7ng/ml ECHO: anteroseptal akinesia in the LVe with severely depressed LV function (EF=28%) Angio: total occlusion in the proximal LAD with collaterals from RCA and LCX
  • Acute Myocardial Infarction after Blunt Chest Trauma in A Young Man ECG: Q wave and 2mm ST segment elevation in V1-6, I and avL Cardiac enzymes: CK-MB was 300, and cTnI 5.7ng/ml ECHO: anteroseptal akinesia in the LVe with severely depressed LV function (EF=28%) Angio: total occlusion in the proximal LAD with collaterals from RCA and LCX
  • Acute Myocardial Infarction after Blunt Chest Trauma in A Young Man ECG: Q wave and 2mm ST segment elevation in V1-6, I and avL Cardiac enzymes: CK-MB was 300, and cTnI 5.7ng/ml ECHO: anteroseptal akinesia in the LVe with severely depressed LV function (EF=28%) Angio: total occlusion in the proximal LAD with collaterals from RCA and LCX

Transcript

  • 1. Learning Modules• ECG Basics• How to Analyze a Rhythm• Normal Sinus Rhythm• Heart Arrhythmias• Diagnosing a Myocardial Infarction• Advanced 12-Lead Interpretation
  • 2. Normal Impulse ConductionSinoatrial node AV node Bundle of HisBundle Branches Purkinje fibers
  • 3. Impulse Conduction & the ECG Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers
  • 4. The “PQRST” • P wave - Atrial depolarization • QRS - Ventricular depolarization • T wave - Ventricular repolarization
  • 5. The PR IntervalAtrial depolarization +delay in AV junction(AV node/Bundle of His)(delay allows time for the atria to contract before the ventricles contract)
  • 6. Pacemakers of the Heart• SA Node - Dominant pacemaker with an intrinsic rate of 60 - 100 beats/minute.• AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute.• Ventricular cells - Back-up pacemaker with an intrinsic rate of 20 - 45 bpm.
  • 7. The ECG Paper• Horizontally – One small box - 0.04 s – One large box - 0.20 s• Vertically – One large box - 0.5 mV
  • 8. The ECG Paper (cont) 3 sec 3 sec• Every 3 seconds (15 large boxes) is marked by a vertical line.• This helps when calculating the heart rate.NOTE: the following strips are not marked but all are 6 seconds long.
  • 9. ECG Rhythm Interpretation How to Analyze a Rhythm
  • 10. Rhythm Analysis• Step 1: Calculate rate.• Step 2: Determine regularity.• Step 3: Assess the P waves.• Step 4: Determine PR interval.• Step 5: Determine QRS duration.
  • 11. Step 1: Calculate Rate 3 sec 3 sec• Option 1 – Count the # of R waves in a 6 second rhythm strip, then multiply by 10. – Reminder: all rhythm strips in the Modules are 6 seconds in length.Interpretation? 9 x 10 = 90 bpm
  • 12. Step 1: Calculate Rate R wave• Option 2 – Find a R wave that lands on a bold line. – Count the # of large boxes to the next R wave. If the second R wave is 1 large box away the rate is 300, 2 boxes - 150, 3 boxes - 100, 4 boxes - 75, etc. (cont)
  • 13. Step 1: Calculate Rate 3 1 1 0 5 0 7 6 5 0 0 0 5 0 0• Option 2 (cont) – Memorize the sequence: 300 - 150 - 100 - 75 - 60 - 50Interpretation? Approx. 1 box less than 100 = 95 bpm
  • 14. Step 2: Determine regularity R R• Look at the R-R distances (using a caliper or markings on a pen or paper).• Regular (are they equidistant apart)? Occasionally irregular? Regularly irregular? Irregularly irregular?Interpretation? Regular
  • 15. Step 3: Assess the P waves• Are there P waves?• Do the P waves all look alike?• Do the P waves occur at a regular rate?• Is there one P wave before each QRS?Interpretation? Normal P waves with 1 P wave for every QRS
  • 16. Step 5: QRS duration• Normal: 0.04 - 0.12 seconds. (1 - 3 boxes)Interpretation? 0.08 seconds
  • 17. Rhythm Summary• Rate 90-95 bpm• Regularity regular• P waves normal• PR interval 0.12 s• QRS duration 0.08 sInterpretation? Normal Sinus Rhythm
  • 18. Step 4: Determine PR interval• Normal: 0.12 - 0.20 seconds. (3 - 5 boxes)Interpretation? 0.12 seconds
  • 19. ECG Rhythm Interpretation Module III Normal Sinus Rhythm
  • 20. Normal Sinus Rhythm (NSR)• Etiology: the electrical impulse is formed in the SA node and conducted normally.• This is the normal rhythm of the heart; other rhythms that do not conduct via the typical pathway are called arrhythmias.
  • 21. NSR Parameters•Rate 60 - 100 bpm•Regularity regular•P waves normal•PR interval 0.12 - 0.20 s•QRS duration 0.04 - 0.12 sAny deviation from above is sinus tachycardia, sinus bradycardia or an arrhythmia
  • 22. Arrhythmia FormationArrhythmias can arise from problems in the: • Sinus node • Atrial cells • AV junction • Ventricular cells
  • 23. SA Node ProblemsThe SA Node can:• fire too slow Sinus Bradycardia• fire too fast Sinus Tachycardia Sinus Tachycardia may be an appropriate response to stress.
  • 24. Atrial Cell ProblemsAtrial cells can:• fire occasionally Premature Atrial from a focus Contractions (PACs)• fire continuously Atrial Flutter due to a looping re-entrant circuit
  • 25. Teaching Moment• A re-entrant pathway occurs when an impulse loops and results in self- perpetuating impulse formation.
  • 26. Atrial Cell ProblemsAtrial cells can also:• fire continuously Atrial Fibrillationfrom multiple fociorfire continuously Atrial Fibrillationdue to multiplemicro re-entrant“wavelets”
  • 27. Teaching Moment Atrial tissueMultiple micro re-entrant “wavelets”refers to wanderingsmall areas ofactivation whichgenerate fine chaoticimpulses. Collidingwavelets can, in turn,generate new foci ofactivation.
  • 28. AV Junctional ProblemsThe AV junction can:• fire continuously Paroxysmal due to a looping Supraventricular re-entrant circuit Tachycardia• block impulses AV Junctional Blocks coming from the SA Node
  • 29. Ventricular Cell ProblemsVentricular cells can:• fire occasionally Premature Ventricular from 1 or more foci Contractions (PVCs)• fire continuously Ventricular Fibrillation from multiple foci• fire continuously Ventricular Tachycardia due to a looping re-entrant circuit
  • 30. End of Module IIINormal Sinus Rhythm
  • 31. ECG Rhythm Interpretation Acute Myocardial Infarction
  • 32. Course Objectives• To recognize the normal rhythm of the heart - “Normal Sinus Rhythm.”• To recognize the 13 most common heart arrhythmias.• To recognize an acute myocardial infarction on a 12-lead ECG.
  • 33. Learning Modules• ECG Basics• How to Analyze a Rhythm• Normal Sinus Rhythm• Heart Arrhythmias• Diagnosing a Myocardial Infarction• Advanced 12-Lead Interpretation
  • 34. Diagnosing a MI To diagnose a myocardial infarction you need to go beyond looking at a rhythm strip and obtain a 12-Lead ECG. 12-Lead ECGRhythmStrip
  • 35. The 12-Lead ECG• The 12-Lead ECG sees the heart from 12 different views.• Therefore, the 12-Lead ECG helps you see what is happening in different portions of the heart.• The rhythm strip is only 1 of these 12 views.
  • 36. The 12-LeadsThe 12-leads include: –3 Limb leads (I, II, III) –3 Augmented leads (aVR, aVL, aVF) –6 Precordial leads (V1- V6)
  • 37. Views of the Heart Lateral portionSome leads get a of the heartgood view of the: Anterior portion of the heart Inferior portion of the heart
  • 38. ST ElevationOne way todiagnose anacute MI is tolook forelevation ofthe STsegment.
  • 39. ST Elevation (cont)Elevation of theST segment(greater than 1small box) in 2leads isconsistent with amyocardialinfarction.
  • 40. Anterior View of the HeartThe anterior portion of the heart is bestviewed using leads V1- V4.
  • 41. Anterior Myocardial InfarctionIf you see changes in leads V1 - V4that are consistent with a myocardialinfarction, you can conclude that it isan anterior wall myocardial infarction.
  • 42. Putting it all TogetherDo you think this person is having amyocardial infarction. If so, where?
  • 43. InterpretationYes, this person is having an acute anteriorwall myocardial infarction.
  • 44. Other MI LocationsNow that you know where to look for ananterior wall myocardial infarction let’slook at how you would determine if the MIinvolves the lateral wall or the inferior wallof the heart.
  • 45. Other MI LocationsFirst, take a look Lateral portionagain at this of the heartpicture of the heart. Anterior portion of the heart Inferior portion of the heart
  • 46. Other MI LocationsSecond, remember that the 12-leads of the ECG look atdifferent portions of the heart. The limb and augmentedleads “see” electrical activity moving inferiorly (II, III andaVF), to the left (I, aVL) and to the right (aVR). Whereas, theprecordial leads “see” electrical activity in the posterior toanterior direction. Limb Leads Augmented Leads Precordial Leads
  • 47. Other MI LocationsNow, using these 3 diagrams let’s figure whereto look for a lateral wall and inferior wall MI. Limb Leads Augmented Leads Precordial Leads
  • 48. Anterior MIRemember the anterior portion of the heart isbest viewed using leads V1- V4. Limb Leads Augmented Leads Precordial Leads
  • 49. Lateral MISo what leads do you thinkthe lateral portion of the Leads I, aVL, and V5- V6heart is best viewed? Limb Leads Augmented Leads Precordial Leads
  • 50. Inferior MINow how about theinferior portion of the Leads II, III and aVFheart? Limb Leads Augmented Leads Precordial Leads
  • 51. Putting it all TogetherNow, where do you think this person ishaving a myocardial infarction?
  • 52. Inferior Wall MIThis is an inferior MI. Note the ST elevationin leads II, III and aVF.
  • 53. Putting it all TogetherHow about now? For more presentations www.medicalppt.blogspot.com
  • 54. Anterolateral MIThis person’s MI involves both the anterior wall(V2-V4) and the lateral wall (V5-V6, I, and aVL)!
  • 55. ECG Rhythm InterpretationAdvanced 12-Lead Interpretation
  • 56. Course Objectives• To recognize the normal rhythm of the heart - “Normal Sinus Rhythm.”• To recognize the 13 most common heart arrhythmias.• To recognize an acute myocardial infarction on a 12-lead ECG.
  • 57. Learning Modules• ECG Basics• How to Analyze a Rhythm• Normal Sinus Rhythm• Heart Arrhythmias• Diagnosing a Myocardial Infarction• Advanced 12-Lead Interpretation
  • 58. The 12-Lead ECGThe 12-Lead ECG contains a wealth ofinformation. In Module V you learned thatST segment elevation in two leads issuggestive of an acute myocardialinfarction. In this module we will cover: – ST Elevation and non-ST Elevation MIs – Left Ventricular Hypertrophy – Bundle Branch Blocks
  • 59. ST Elevation andnon-ST Elevation MIs
  • 60. ST Elevation and non-ST Elevation MIs• When myocardial blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events occur beginning with ischemia (inadequate tissue perfusion), followed by necrosis (infarction), and eventual fibrosis (scarring) if the blood supply isnt restored in an appropriate period of time.• The ECG changes over time with each of these events…
  • 61. ECG ChangesWays the ECG can change include: ST elevation & depression T-waves peaked flattenedAppearance invertedof pathologicQ-waves
  • 62. ECG Changes & the Evolving MIThere are two Non-ST Elevationdistinct patternsof ECG changedepending if theinfarction is: ST Elevation–ST Elevation (Transmural or Q-wave), or–Non-ST Elevation (Subendocardial or non-Q-wave)
  • 63. ST Elevation InfarctionThe ECG changes seen with a ST elevation infarction are: Before injury Normal ECG Ischemia ST depression, peaked T-waves, then T-wave inversion Infarction ST elevation & appearance of Q-waves Fibrosis ST segments and T-waves return to normal, but Q-waves persist
  • 64. ST Elevation InfarctionHere’s a diagram depicting an evolving infarction:A. Normal ECG prior to MIB. Ischemia from coronary artery occlusion results in ST depression (not shown) and peaked T-wavesC. Infarction from ongoing ischemia results in marked ST elevationD/E. Ongoing infarction with appearance of pathologic Q-waves and T-wave inversionF. Fibrosis (months later) with persistent Q- waves, but normal ST segment and T- waves
  • 65. ST Elevation InfarctionHere’s an ECG of an inferior MI:Look at theinferior leads(II, III, aVF).Question:What ECGchanges doyou see?ST elevationand Q-wavesExtra credit:What is therhythm? Atrial fibrillation (irregularly irregular with narrow QRS)!
  • 66. Non-ST Elevation InfarctionHere’s an ECG of an inferior MI later in time:Now what doyou see in theinferior leads?ST elevation,Q-waves andT-waveinversion
  • 67. Non-ST Elevation InfarctionThe ECG changes seen with a non-ST elevation infarction are:Before injury Normal ECGIschemia ST depression & T-wave inversionInfarction ST depression & T-wave inversionFibrosis ST returns to baseline, but T-wave inversion persists
  • 68. Non-ST Elevation InfarctionHere’s an ECG of an evolving non-ST elevation MI:Note the STdepressionand T-waveinversion inleads V2-V6.Question:What area ofthe heart isinfarcting?Anterolateral
  • 69. Left Ventricular Hypertrophy
  • 70. Left Ventricular Hypertrophy Compare these two 12-lead ECGs. What stands out as different with the second one? Normal Left Ventricular HypertrophyAnswer:
  • 71. Left Ventricular HypertrophyWhy is left ventricular hypertrophy characterized by tallQRS complexes? As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage. LVH ECHOcardiogram Increased QRS voltage
  • 72. Left Ventricular Hypertrophy• Criteria exists to diagnose LVH using a 12-lead ECG. – For example: • The R wave in V5 or V6 plus the S wave in V1 or V2 exceeds 35 mm.• However, for now, all you need to know is that the QRS voltage increases with LVH.
  • 73. Bundle Branch Blocks
  • 74. Bundle Branch BlocksTurning our attention to bundle branch blocks… Remember normal impulse conduction is SA node  AV node  Bundle of His  Bundle Branches  Purkinje fibers
  • 75. Normal Impulse ConductionSinoatrial node AV node Bundle of HisBundle Branches Purkinje fibers
  • 76. Bundle Branch BlocksSo, depolarization ofthe Bundle Branchesand Purkinje fibers areseen as the QRScomplex on the ECG.Therefore, a conductionblock of the BundleBranches would be Rightreflected as a change in BBBthe QRS complex.
  • 77. Bundle Branch BlocksWith Bundle Branch Blocks you will see two changeson the ECG. 1. QRS complex widens (> 0.12 sec). 2. QRS morphology changes (varies depending on ECG lead, and if it is a right vs. left bundle branch block).
  • 78. Bundle Branch BlocksWhy does the QRS complex widen?When the conductionpathway is blocked itwill take longer forthe electrical signalto pass throughoutthe ventricles.
  • 79. Right Bundle Branch BlocksWhat QRS morphology is characteristic?For RBBB the wide QRS complex assumes aunique, virtually diagnostic shape in thoseleads overlying the right ventricle (V1 and V2). V1 “Rabbit Ears”
  • 80. Left Bundle Branch BlocksWhat QRS morphology is characteristic?For LBBB the wide QRS complex assumes acharacteristic change in shape in those leadsopposite the left ventricle (right ventricularleads - V1 and V2). Broad,Normal deep S waves
  • 81. SummaryThis Module introduced you to: – ST Elevation and Non-ST Elevation MIs – Left Ventricular Hypertrophy – Bundle Branch BlocksDon’t worry too much right now about trying toremember all the details. You’ll focus more onadvanced ECG interpretation in your clinicalyears!
  • 82. End of Module VI Advanced 12-Lead InterpretationProceed to Module VI Practice Quiz on WebCT
  • 83. ECG Rhythm Interpretation Reading 12-Lead ECG’s
  • 84. Course Objective• To systematically analyze a 12-lead ECG.
  • 85. Learning Modules• ECG Basics• How to Analyze a Rhythm• Normal Sinus Rhythm• Heart Arrhythmias• Diagnosing a Myocardial Infarction• Advanced 12-Lead Interpretation• Reading 12-Lead ECG’s
  • 86. Reading 12-Lead ECGs• The 12-Lead ECG contains information that will assistyou in making diagnostic and treatment decisions in yourclinical practice. In previous modules you learned how toread and interpret parts of the ECG. Now, we will bring allthat you have learned together so that you cansystematically read and interpret a 12-lead ECG.• The information will be divided into two modules, VII aand VII b.
  • 87. Reading 12-Lead ECGsThe best way to read 12-lead ECGs is to develop a step-by-step approach (just as we did for analyzing a rhythmstrip). In these modules we present a 6-step approach: 1. Calculate RATE 2. Determine RHYTHM 3. Determine QRS AXIS 4. Calculate INTERVALS 5. Assess for HYPERTROPHY 6. Look for evidence of INFARCTION
  • 88. Rate Rhythm Axis Intervals Hypertrophy Infarct• In Module II you learned how to calculate therate. If you need a refresher return to that module.• There is one new thing to keep in mind whendetermining the rate in a 12-lead ECG…
  • 89. Rate Rhythm Axis Intervals Hypertrophy InfarctIf you use the rhythmstrip portion of the12-lead ECG the totallength of it is always10 seconds long. Soyou can count thenumber of R wavesin the rhythm stripand multiply by 6 todetermine the beatsper minute. Rate? 12 (R waves) x 6 = 72 bpm
  • 90. Rate Rhythm Axis Intervals Hypertrophy Infarct• In Module II you learned how to systematicallyanalyze a rhythm by looking at the rate, regularity,P waves, PR interval and QRS complexes.• In Modules III, IV and V you learned how torecognize Normal Sinus Rhythm and the 13 mostcommon rhythm disturbances.• If you need a refresher return to these modules.
  • 91. Rate Rhythm Axis Intervals Hypertrophy Infarct Tip: the rhythm strip portion of the 12-lead ECG is a good place to look at when trying to determine the rhythm because the 12 leads only capture a few beats. Rhythm? Atrial1 of 12 fibrillationleads Lead IIRhythmstrip
  • 92. Rate Rhythm Axis Intervals Hypertrophy InfarctAxis refers to the mean QRS axis (or vector) during ventriculardepolarization. As you recall when the ventricles depolarize (in anormal heart) the direction of current flows leftward and downwardbecause most of the ventricular mass is in the left ventricle. We liketo know the QRS axis because an abnormal axis can suggestdisease such as pulmonary hypertension from a pulmonaryembolism.
  • 93. Rate Rhythm Axis Intervals Hypertrophy InfarctThe QRS axis is determined by overlying a circle, in the frontalplane. By convention, the degrees of the circle are as shown.The normal QRS axis lies between -30oand +90o. that fallsA QRS axis -90o -120 o -60o o obetween -30 and -90 is o -150abnormal and called left -30oA QRS axis that fallsaxis deviation. o 0obetween +90o and +150o is 180abnormal and called right 150 o 30oA QRS axis that fallsaxis deviation. obetween +150 and -90o is 120 o 60o 90oabnormal and called superiorright axis deviation.
  • 94. For more presentations www.medicalppt.blogspot.com
  • 95. Rate Rhythm Axis Intervals Hypertrophy InfarctWe can quickly determine whether the QRS axis isnormal by looking at leads I and II. QRS negative (R < Q+S)If the QRS complex isoverall positive (R > Q+S)in leads I and II, the QRSaxis is normal.In this ECG what leadshave QRS complexesthat are negative?equivocal? QRS equivocal (R = Q+S)
  • 96. Rate Rhythm Axis Intervals Hypertrophy Infarct How do we know the axis is normal when the QRS complexes are positive in leads I and II?
  • 97. Rate Rhythm Axis Intervals Hypertrophy InfarctThe answer lies in the fact that each frontal leadcorresponds to a location on the circle.Limb leads -90o I = +0o -120o -60o II = +60o av -150o -30o av o III = +120 R L Augmented leads 180o 0o II avL = -30o 30o 150o avF = +90o 60o avR = -150 o 120o III 90o IIII av
  • 98. Rate Rhythm Axis Intervals Hypertrophy InfarctSince lead I is orientated at 0o a wave of depolarization directed towards itwill result in a positive QRS axis. Therefore any mean QRS vectorbetween -90o and +90o will be positive. -90o -120o -60o -150o -30o 180o 0o I 150o 30o o 60o 120 90o
  • 99. Rate Rhythm Axis Intervals Hypertrophy InfarctSince lead I is orientated at 0o a wave of depolarization directed towards itwill result in a positive QRS axis. Therefore any mean QRS vectorbetween -90o and +90o will be positive.Similarly, since lead II is -90o -120 o -60oorientated at 60o a wave of odepolarization directed towards -150 -30oit will result in a positive QRS 180axis. Therefore any mean QRS o 0o Ivector between -30o and +150o 150 o 30owill be positive. 60o o 120 90o II
  • 100. Rate Rhythm Axis Intervals Hypertrophy InfarctSince lead I is orientated at 0o a wave of depolarization directed towards itwill result in a positive QRS axis. Therefore any mean QRS vectorbetween -90o and +90o will be positive.Similarly, since lead II is -90o -120 o -60oorientated at 60o a wave of odepolarization directed towards -150 -30oit will result in a positive QRS 180axis. Therefore any mean QRS o 0o ITherefore, if the QRS complexvector between -30o andI +150o 150is positive in both leads and o 30owill be positive. must beII the QRS axis 60o o o o 120between -30 and 90 (where 90o IIleads I and II overlap) and, asa result, the axis must be
  • 101. Rate Rhythm Axis Intervals Hypertrophy InfarctNow using what you just learned fill in the following table. For example, ifthe QRS is positive in lead I and negative in lead II what is the QRS axis?(normal, left, right or right superior axis deviation)QRS Complexes -90o I II Axis -120o -60o + + normal -150o -30o + - left axis deviation 180o 0o I 150o 30o o 60o 120 90o II
  • 102. Rate Rhythm Axis Intervals Hypertrophy Infarct… if the QRS is negative in lead I and positive in lead II what is the QRSaxis? (normal, left, right or right superior axis deviation)QRS Complexes -90o I II Axis -120o -60o + + normal -150o -30o + - left axis deviation - + right axis deviation 180o 0o I 150o 30o o 60o 120 90o II
  • 103. Rate Rhythm Axis Intervals Hypertrophy Infarct… if the QRS is negative in lead I and negative in lead II what is the QRSaxis? (normal, left, right or right superior axis deviation)QRS Complexes -90o I II Axis -120o -60o + + normal -150o -30o + - left axis deviation - + right axis deviation 180o 0o I - - right superior 150o 30o axis deviation o 60o 120 90o II
  • 104. Rate Rhythm Axis Intervals Hypertrophy InfarctIs the QRS axis normal in this ECG? No, there is left axis deviation. The QRS is positive in I and negative in II.
  • 105. Rate Rhythm Axis Intervals Hypertrophy InfarctTo summarize: – The normal QRS axis falls between -30o and +90o because ventricular depolarization is leftward and downward. – Left axis deviation occurs when the axis falls between -30o and -90o. – Right axis deviation occurs when the axis falls between +90o and +150o. – Right superior axis deviation occurs when the axis falls between between +150o and -90o. – A quick way to QRS Complexes I II Axis determine + + normal the QRS + - left axis deviation axis is to look at the - + right axis deviation QRS complexes in - - right superior axis deviation leads I and II.
  • 106. SUMMARY Rate Rhythm Axis Intervals Hypertrophy InfarctTo summarize VII a: 1. Calculate RATE 2. Determine RHYTHM 3. Determine QRS AXIS – Normal – Left axis deviation – Right axis deviation – Right superior axis deviation
  • 107. SUMMARY Rate Rhythm Axis Intervals Hypertrophy InfarctIn VII b we will cover the next 3 steps: 1. Calculate RATE 2. Determine RHYTHM 3. Determine QRS AXIS 4. Calculate INTERVALS 5. Assess for HYPERTROPHY 6. Look for evidence of INFARCTION
  • 108. ECG Rhythm Interpretation Reading 12-Lead ECG’s
  • 109. Course Objective• To systematically analyze a 12-lead ECG.
  • 110. Learning Modules• ECG Basics• How to Analyze a Rhythm• Normal Sinus Rhythm• Heart Arrhythmias• Diagnosing a Myocardial Infarction• Advanced 12-Lead Interpretation• Reading 12-Lead ECG’s
  • 111. Reading 12-Lead ECGsIn Module VII a we introduced a 6 step approach foranalyzing a 12-lead ECG and covered the first 3 steps. Inthis module we will cover the last 3 steps. 1. Calculate RATE 2. Determine RHYTHM 3. Determine QRS AXIS 4. Calculate INTERVALS 5. Assess for HYPERTROPHY 6. Look for evidence of INFARCTION
  • 112. Rate Rhythm Axis Intervals Hypertrophy Infarct• Intervals refers to the length of the PR and QT intervalsand the width of the QRS complexes. You should havealready determined the PR and QRS during the “rhythm”step, but if not, do so in this step.• In the following few slides we’ll review what is a normaland abnormal PR, QRS and QT interval. Also listed are afew common causes of abnormal intervals.
  • 113. Rate Rhythm Axis Intervals Hypertrophy InfarctPR interval < 0.12 s 0.12-0.20 s > 0.20 s High catecholamine states Normal AV nodal blocks Wolff-Parkinson-White Wolff-Parkinson-White 1st Degree AV Block
  • 114. Rate Rhythm Axis Intervals Hypertrophy InfarctQRS complex < 0.10 s 0.10-0.12 s > 0.12 s Bundle branch block Incomplete bundle Normal PVC branch block Ventricular rhythm Incomplete bundle branch block 3rd degree AV block with ventricular escape rhythm Remember: If you have a BBB determine if it is a right or left BBB. If you need a refresher see Module VI.
  • 115. Rate Rhythm Axis Intervals Hypertrophy InfarctQT intervalThe duration of the QT interval isproportionate to the heart rate. The fasterthe heart beats, the faster the ventriclesrepolarize so the shorter the QT interval.Therefore what is a “normal” QT varieswith the heart rate. For each heart rate youneed to calculate an adjusted QT interval,called the “corrected QT” (QTc): QTc = QT / square root of RR interval
  • 116. Rate Rhythm Axis Intervals Hypertrophy InfarctQTc interval < 0.44 s > 0.44 s Long QT Normal Long QT Torsades de PointesA prolonged QT can be very dangerous. It may predispose an individual to a type ofventricular tachycardia called Torsades de Pointes. Causes include drugs, electrolyteabnormalities, CNS disease, post-MI, and congenital heart disease.
  • 117. Rate Rhythm Axis Intervals Hypertrophy Infarct QT = 0.40 s RR = 0.68 s Square root of RR = 0.82 QTc = 0.40/0.82 = 0.49 sPR QRS QTc 0.16interval? 0.08 width? 0.49 interval?Interpretation of seconds PR and QRS, long seconds Normal secondsintervals? QT
  • 118. Rate Rhythm Axis Intervals Hypertrophy Infarct RR 23 boxes 17 boxes 10 boxes 13 boxes QT Normal QT Long QTTip: Instead of calculating the QTc, a quick wayto estimate if the QT interval long is to use thefollowing rule: A QT > half of the RR interval is probably long.
  • 119. Rate Rhythm Axis Intervals Hypertrophy InfarctIn this step of the 12-lead ECG analysis, we use the ECGto determine if any of the 4 chambers of the heart areenlarged or hypertrophied. We want to determine if thereare any of the following: – Right atrial enlargement (RAE) – Left atrial enlargement (LAE) – Right ventricular hypertrophy (RVH) – Left ventricular hypertrophy (LVH)
  • 120. Rate Rhythm Axis Intervals Hypertrophy Infarct• In Module VI we introduced the concept of left ventricularhypertrophy. As you remember the QRS voltage increases with LVHand is characterized by tall QRS complexes in certain leads. Similarlyfor right ventricular hypertrophy we look at the QRS complexes forchanges in voltage patterns.• With right and left atrial enlargement we analyze the P wave (sincethe P wave represents atrial depolarization). Here we also look forchanges in voltage patterns.• Note: as mentioned in Module VI criteria exists to diagnose LVH,the same goes for RAE, LAE and RVH. In the following slides we willbe presenting criteria you can use. However other criteria exists andas a reference you might find it useful to carry a copy of Tom Evans’ECG Interpretation Cribsheet.
  • 121. Rate Rhythm Axis Intervals Hypertrophy InfarctRight atrial enlargement – Take a look at this ECG. What do you notice about the P waves? The P waves are tall, especially in leads II, III and avF. Ouch! They would hurt to
  • 122. Rate Rhythm Axis Intervals Hypertrophy InfarctRight atrial enlargement – To diagnose RAE you can use the following criteria: • II P > 2.5 mm, or • V1 or V2 P > 1.5 mm > 1 ½ boxes (in height) Remember 1 small > 2 ½ boxes (in height) box in height = 1 mm A cause of RAE is RVH from pulmonary hypertension.
  • 123. Rate Rhythm Axis Intervals Hypertrophy InfarctLeft atrial enlargement – Take a look at this ECG. What do you notice about the P waves? Notched Negative deflection The P waves in lead II are notched and in lead V1 they have a deep and wide
  • 124. Rate Rhythm Axis Intervals Hypertrophy InfarctLeft atrial enlargement – To diagnose LAE you can use the following criteria: • II > 0.04 s (1 box) between notched peaks, or • V1 Neg. deflection > 1 box wide x 1 box deep Normal LAE A common cause of LAE is LVH from hypertension.
  • 125. Rate Rhythm Axis Intervals Hypertrophy InfarctRight ventricular hypertrophy – Take a look at this ECG. What do you notice about the axis and QRS complexes over the right ventricle (V1, V2)? There is right axis deviation (negative in I, positive in II) and there are tall R waves in
  • 126. Rate Rhythm Axis Intervals Hypertrophy InfarctRight ventricular hypertrophy – Compare the R waves in V1, V2 from a normal ECG and one from a person with RVH. – Notice the R wave is normally small in V1, V2 because the right ventricle does not have a lot of muscle mass. – But in the hypertrophied right ventricle the R wave is tall in V1, V2. Normal RVH
  • 127. Rate Rhythm Axis Intervals Hypertrophy InfarctRight ventricular hypertrophy – To diagnose RVH you can use the following criteria: • Right axis deviation, and • V1 R wave > 7mm tall A common cause of RVH is left heart failure.
  • 128. Rate Rhythm Axis Intervals Hypertrophy InfarctLeft ventricular hypertrophy – Take a look at this ECG. What do you notice about the axis and QRS complexes over the left ventricle (V5, V6) and right ventricle (V1, V2)? The deep S waves seen in the leads over the right ventricle are created because the heart is depolarizing left, superior and posterior (away from leads V1, V2). There is left axis deviation (positive in I, negative in II) and there are tall R waves in V5, V6 and
  • 129. Rate Rhythm Axis Intervals Hypertrophy InfarctLeft ventricular hypertrophy – To diagnose LVH you can use the following criteria*: • R in V5 (or V6) + S in V1 (or V2) > 35 mm, or • avL R > 13 mm S = 13 mm * There are several other criteria for the diagnosis of LVH. R = 25 mm A common cause of LVH is hypertension.
  • 130. Rate Rhythm Axis Intervals Hypertrophy InfarctA 63 yo man has longstanding, uncontrolled hypertension. Is there evidenceof heart disease from his hypertension? (Hint: There a 3 abnormalities.) Yes, there is left axis deviation (positive in I, negative in II), left atrial enlargement (> 1 x 1 boxes in V1) and LVH (R in V5 = 27 + S in V2 = 10  > 35 mm).
  • 131. Rate Rhythm Axis Intervals Hypertrophy Infarct• When analyzing a 12-lead ECG for evidence of aninfarction you want to look for the following: – Abnormal Q waves – ST elevation or depression – Peaked, flat or inverted T waves• These topics were covered in Modules V and VI whereyou learned: – ST elevation (or depression) of 1 mm in 2 or more contiguous leads is consistent with an AMI – There are ST elevation (Q-wave) and non-ST elevation (non-Q wave) MIs
  • 132. Rate Rhythm Axis Intervals Hypertrophy InfarctTip: One way to determine if Q waves (and R waves) are abnormal is bylooking at the width and using the following mantra (read red downwards): Any Any Q wave in V1 Any Any Q wave in V2 Any Any Q wave in V3 20 A Q wave > 20 msec in V4 (i.e. 0.02 sec or ½ width of a box) 30 A Q wave > 30 msec in V5 30 A Q wave > 30 msec in V6 30 A Q wave > 30 msec in I 30 A Q wave > 30 msec in avL 30 A Q wave > 30 msec in II 30 A Q wave > 30 msec in avF R40 A R wave > 40 msec in V1 R50 A R wave > 50 msec in V2
  • 133. Rate Rhythm Axis Intervals Hypertrophy InfarctThis mantra corresponds to the ECG in the following way: 30 Any R40 20 30 30 Any R50 30 30 Any 30
  • 134. SUMMARY Rate Rhythm Axis Intervals Hypertrophy InfarctTo summarize: 1. Calculate RATE 2. Determine RHYTHM 3. Determine QRS AXIS – Normal – Left axis deviation – Right axis deviation – Right superior axis deviation
  • 135. SUMMARY Rate Rhythm Axis Intervals Hypertrophy InfarctTo summarize: 1. Calculate RATE 2. Determine RHYTHM 3. Determine QRS AXIS 4. Calculate INTERVALS – PR – QRS – QT
  • 136. SUMMARY Rate Rhythm Axis Intervals Hypertrophy InfarctTo summarize: 1. Calculate RATE 2. Determine RHYTHM 3. Determine QRS AXIS 4. Calculate INTERVALS 5. Assess for HYPERTROPHY – Right and left atrial enlargement – Right and left ventricular hypertrophy
  • 137. SUMMARY Rate Rhythm Axis Intervals Hypertrophy InfarctTo summarize: 1. Calculate RATE 2. Determine RHYTHM 3. Determine QRS AXIS 4. Calculate INTERVALS 5. Assess for HYPERTROPHY 6. Look for evidence of INFARCTION – Abnormal Q waves – ST elevation or depression – Peaked, flat or inverted T waves
  • 138. SUMMARY Rate Rhythm Axis Intervals Hypertrophy InfarctTo summarize: 1. Calculate RATE 2. Determine RHYTHM 3. Determine QRS AXIS 4. Calculate INTERVALS 5. Assess for HYPERTROPHY 6. Look for evidence of INFARCTIONNow to finish this module lets analyze a 12-lead ECG!
  • 139. SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct A 16 yo young man ran into a guardrail while riding a motorcycle. In the ED he is comatose and dyspneic. This is his ECG.
  • 140. SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct What is the rate? Approx. 132 bpm (22 R waves x 6)
  • 141. SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct What is the rhythm? Sinus tachycardia
  • 142. SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct What is the QRS axis? Right axis deviation (- in I, + in II)
  • 143. SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct What are the PR, QRS PR = 0.12 s, QRS = 0.08 s, QTc = 0.482 s and QT intervals?
  • 144. SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct Is there evidence of No (no peaked, notched or negatively atrial enlargement? deflected P waves)
  • 145. SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct Is there evidence of No (no tall R waves in V1/V2 or V5/V6) ventricular hypertrophy?
  • 146. SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct Infarct: Are there abnormal Yes! In leads V1-V6 and I, avL Q waves? 30 Any R40 20 30 30 Any R50 30 30 Any 30
  • 147. SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct Infarct: Is the ST elevation Yes! Elevation in V2-V6, I and avL. or depression? Depression in II, III and avF.
  • 148. SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct Infarct: Are there T wave No changes?
  • 149. SUMMARY Rate Rhythm Axis Intervals Hypertrophy Infarct ECG analysis: Sinus tachycardia at 132 bpm, right axis deviation, long QT, and evidence of ST elevation infarction in the anterolateral leads (V1-V6, I, avL) with reciprocal changes (the ST depression) in the inferior leads (II, III, avF). This young man suffered an acute myocardial infarction after blunt trauma. An echocardiogram showed anteroseptal akinesia in the left ventricle with severely depressed LV function (EF=28%). An angiogram showed total